Tuberculosis and Respiratory Diseases

The Korean Academy of Tuberculosis and Respiratory Diseases (대한결핵및호흡기학회)
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Regulation of Tumor Necrosis Factor-${\alpha}$-induced Airway Mucin Production and Gene Expression by Carbenoxolone, Prunetin, and Silibinin

  • Lee, Hyun-Jae (Department of Pharmacology, Chungnam National University School of Medicine) ;
  • Lee, Su-Yel (Department of Pharmacology, Chungnam National University School of Medicine) ;
  • Jeon, Byeong-Kyou (Department of Radiologic Technology, Daegu Health College) ;
  • Lee, Jae-Woo (LG Life Science) ;
  • Lee, Mi-Nam (Department of Pharmacology, Chungnam National University School of Medicine) ;
  • Kim, Ju-Ock (Pulmonology Section, Department of Internal Medicine, Chungnam National University Hospital, Chungnam National University School of Medicine) ;
  • Lee, Choong-Jae (Department of Pharmacology, Chungnam National University School of Medicine)
  • Received : 2010.08.24
  • Accepted : 2010.09.14
  • Published : 2010.11.30
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Abstract

Background: In this study, we tried to investigate whether carbenoxolone, prunetin, and silibinin affect tumor necrosis factor (TNF)-${\alpha}$-induced MUC5AC mucin production and gene expression from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with each agent (carbenoxolone, prunetin, and silibinin) for 30 min and then stimulated with TNF-${\alpha}$ for 24 hours. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay, respectively. Results: Carbenoxolone, prunetin and silibinin inhibited the production of MUC5AC mucin protein induced by TNF-${\alpha}$; the 3 compounds also inhibited the expression of MUC5AC mucin gene induced by TNF-${\alpha}$. Conclusion: This result suggests that carbenoxolone, prunetin and silibinin can inhibit mucin gene expression and production of mucin protein induced by TNF-${\alpha}$, by directly acting on airway epithelial cells.

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